Tumor Growth Rate In Patients Research Articles

Kidney scoring surveillance: predictive machine learning models for clear cell renal cell carcinoma growth using MRI.

Classification of clear cell renal cell carcinoma (ccRCC) growth rates in patients with Von Hippel-Lindau (VHL) syndrome has several ramifications for tumor monitoring and surgical planning. Using two separate machine-learning algorithms, we sought to produce models to predict ccRCC growth rate classes based on qualitative MRI-derived characteristics. We used a prospectively maintained database of patients with VHL who underwent surgical resection for ccRCC between January 2015 and June 2022. We employed a threshold growth rate of 0.5cm per year to categorize ccRCC tumors into two distinct groups-'slow-growing' and 'fast-growing'. Utilizing a questionnaire of qualitative imaging features, two radiologists assessed each lesion on different MRI sequences. Two machine-learning models, a stacked ensemble technique and a decision tree algorithm, were used to predict the tumor growth rate classes. Positive predictive value (PPV), sensitivity, and F1-score were used to evaluate the performance of the models. This study comprises 55 patients with VHL with 128 ccRCC tumors. Patients' median age was 48years, and 28 patients were males. Each patient had an average of two tumors, with a median size of 2.1cm and a median growth rate of 0.35cm/year. The overall performance of the stacked and DT model had 0.77 ± 0.05 and 0.71 ± 0.06 accuracies, respectively. The best stacked model achieved a PPV of 0.92, a sensitivity of 0.91, and an F1-score of 0.90. This study provides valuable insight into the potential of machine-learning analysis for the determination of renal tumor growth rate in patients with VHL. This finding could be utilized as an assistive tool for the individualized screening and follow-up of this population.

Change in volumetric tumor growth rate after cytotoxic therapy is predictive of overall survival in recurrent glioblastoma.

Alterations in tumor growth rate (TGR) in recurrent glioblastoma (rGBM) after treatment may be useful for identifying therapeutic activity. The aim of this study was to assess the impact of volumetric TGR alterations on overall survival (OS) in rGBM treated with chemotherapy with or without radiation therapy (RT). Sixty-one rGBM patients treated with chemotherapy with or without concomitant radiation therapy (RT) at 1st or 2nd recurrence were retrospectively examined. Pre- and post-treatment contrast enhancing volumes were computed. Patients were considered "responders" if they reached progression-free survival at 6 months (PFS6) and showed a decrease in TGR after treatment and "non-responders" if they didn't reach PFS6 or if TGR increased. Stratification by PFS6 and based on TGR resulted in significant differences in OS both for all patients and for patients without RT (P < 0.05). A decrease of TGR (P = 0.009), smaller baseline tumor volume (P = 0.02), O6-methylguanine-DNA methyltransferase promoter methylation (P = 0.048) and fewer number of recurrences (P = 0.048) were significantly associated with longer OS after controlling for age, sex and concomitant RT. A decrease in TGR in patients with PFS6, along with smaller baseline tumor volume, were associated with a significantly longer OS in rGBM treated with chemotherapy with or without radiation. Importantly, all patients that exhibited PFS6 also showed a measurable decrease in TGR.

Evaluating the safety of perioperative dexamethasone treatment: A retrospective analysis of a single center pediatric low-grade glioma cohort.

In addition to surgical management, corticosteroids have proven to be beneficial in the management of acute symptoms related to CNS tumors, and have been widely used for many decades, with dexamethasone (DM) representing the most commonly used agent. However, lately published in vitro data possibly indicates a DM-induced suppression of oncogene-induced senescence (OIS) in a preclinical pediatric low-grade glioma (pLGG) model, which, alongside data associating perioperative DM treatment with reduced event-free survival in adult glioma, raises questions concerning the safety of DM treatment in pLGG. A total of 172 patients with pLGG were retrospectively analyzed concerning the impact of perioperative DM application on postoperative short- and long-term tumor growth velocity and progression-free survival (PFS). Three-dimensional volumetric analyses of sequential MRI follow-up examinations were used for assessment of tumor growth behavior. Mean follow-up period accounted for 60.1months. Sixty-five patients (45%) were perioperatively treated with DM in commonly used doses. Five-year PFS accounted for 93% following gross-total resection (GTR) and 57% post incomplete resection (IR). Comparison of short- and long-term postoperative tumor growth rates in patients with vs without perioperative DM application showed no significant difference (short-term: 0.022 vs 0.023 cm3 /month, respectively; long-term: 0.019 vs 0.023 cm3 /month, respectively). Comparison of PFS post IR (5-year-PFS: 65% vs 55%, respectively; 10-year-PFS: 52% vs 53%, respectively) and GTR (5- and 10-years-PFS: 91% vs 92%, respectively) likewise showed similarity. This data emphasizes the safety of perioperative DM application in pLGG, adding further evidence for decision making and requested future guidelines.

LGG-59. Identifying hidden drivers of low-grade glioma tumor growth

Genomic drivers of pediatric low-grade gliomas (pLGGs) converge on alterations that activate the MAPK pathway. However, expression of individual driver oncogenes fails to induce tumor formation with high penetrance and, paradoxically, expression of these oncogenes suppresses growth in vitro. This, combined with the non-monotonic tumor growth rate in patients, suggests that there are “hidden drivers” beyond a single driver oncogene that are necessary to support tumor growth. The goal of this project is to leverage high-throughput functional genomics strategies to identify these hidden drivers of pLGG. Our preliminary data indicates that genes which modulate differentiation are required for the survival of LGG cells, suggesting that these genes may be hidden drivers of LGG tumor growth. Additionally, we hypothesize that secreted factors in the tumor microenvironment regulate pLGG tumor growth, potentially by modulating differentiation. In total, genes which cooperate with pLGG driver oncogenes to promote tumor growth may represent a new class of therapeutic targets and may explain the complex patterns of tumor growth that are observed in patients.

3D-volumetric assessment of response to ivosidenib in IDH-mutant gliomas.

2063 Background: Isocitrate Dehydrogenase (IDH) mutant gliomas represent a distinct class of primary brain tumors. Mutant IDH is a driver mutation implicated in gliomagenesis and a potential therapeutic target. Ivosidenib, an inhibitor of mutant IDH1, is currently being evaluated to treat gliomas. In the present study we assess our single-institutional experience with the off-label use of ivosidenib to reduce tumor growth rate in patients with IDH mutant gliomas. Methods: We have longitudinally analyzed the imaging of patients with histology-proven radio- and chemotherapy-naïve IDH-mutant WHO Grade 2 and 3 astrocytomas (AS) and oligodendrogliomas (OG) treated with off-label ivosidenib between 2019 and 2022. First, each patients’ FLAIR images were anonymized, bias-corrected, co-registered and semi-automatically segmented for volumetric analysis using 3D Slicer 4.11. MR acquisition dates were hidden, and the order of scans was randomized to prevent expectation bias. Volumetric trends and PFS were analyzed. Progressive disease was defined as a ≥40% increase in volume from baseline as per modified RANO criteria. Results: Eleven patients were included in the analysis (median age 46 years [range 26-62], 2F, 8AS/3OG, 7 Grade 2). Mean±SD follow-up time on ivosidenib was 16.1±15.5 months. Tumor volume reduction was noted in 82% of patients at least at one time point. Average volume change at best response was -11.4±12.8%. Mean time to best response was 12.1±9.3 months. PFS-6 and PFS-12 were 91% (n = 11), and 88% (n = 8), respectively. Mean PFS was 24.4 months (CI95% 18.8-29.9). Median PFS was not reached. Patients older than 45 years had significantly higher volume reduction compared to younger patients (18.9±6.3% vs. -2.4±13.2%;-p = 0.047, 2-tailed T-test). Ivosidenib was discontinued in in 2 patients for 2D radiographic changes, and in one for increased seizure frequency. Conclusions: The use of ivosidenib in treatment-naïve gliomas was associated with a high response rate; however, on average it required longer than a year to achieve best response. In this cohort, older patients had higher volume reduction. The drug was well tolerable. Further analysis of an expanded cohort is underway.

Renal tumor growth rate in patients with previously normal CT scan: Analysis of the initial stage of growth.

Most of the studies regarding natural history of renal masses are based on active surveillance series and suggest that the renal masses have a slow growth rate. Nevertheless, only a few studies report the time between a normal computed tomography (CT) scan to the first detection of a tumor. We aimed to analyze the growth rate in newly diagnosed kidney tumors. We analyzed patients with enhancing renal masses that developed after a normal CT scan, which was performed at most 12 months earlier. Variables examined included patient age, gender, tumor size, volume, tumor linear growth rate (LGR). All cases were surgically treated. Mann-Whitney U test was used to compare variables. A p<0.05 was considered as statistically significant. We found 31 patients with 33 lesions. Male to female ratio was 1.58 (19/12). The average age was 59.2 years (standard deviation [SD]±12.1), and the mean tumor size was 4.27 cm (SD±4.3). Tumor LGR was 0.87 cm/month (range: 0.28-1.66) and presumed to be 10.4 cm at 1 year (range: 3.36-19.9). Tumor LGR for time detection at <6 month or ≥6 months were 1.1 cm/month and 0.68 cm/month (range: 0.27-1.08 and 0.88-1.76, respectively; p=0.0004), respectively. Tumor LGRs for low- and high-grade tumors were 0.89 cm/month and 0.83 cm/month (p=0.65), respectively. Median volume was 36.1 cm3 (range: 2.61-143.7), and for low and high grade the median volumes were 27.9 cm3 and 47.6 cm3, respectively (p=0.54). Malignant pathology was present in 93.9 % (31 of 33) of masses (lesions). We found differences in tumor LGR in tumors detected before and after 6 months. We did not find any correlation between tumor growth rate and Fuhrman grade system, gender, histology, or age. We found the highest LGR published up to date.

Abstract 44: TTFields dose distribution alters tumor growth patterns: An imaging-based analysis of the randomized phase 3 EF-14 trial

Abstract Introduction: The pivotal phase 3 EF-14 trial revealed extended Overall Survival (OS) and Progression Free Survival (PFS) in newly Diagnosed Glioblastoma (ndGBM) patients that received Tumor Treating Fields + chemoradiation vs. patients that received chemoradiation alone. The effect of TTFields is dose-dependent, with improved outcomes for patients who received higher doses of TTFields to the tumor bed [1]. Recent studies have also shown that TTFields influences tumor progression patterns in patients in a dose-dependent manner, with recurrence more likely to occur in regions of the brain in which field intensities are lower. This study also revealed that distal progressions are more common in ndGBM patients treated with TTFields_chemoradiation vs. patients treated with chemoradiation alone [2]. Thus it seems that a major influence of TTFields is to enhance local control of the primary lesion. Here we present an analysis testing this hypothesis by analyzing tumor growth rates in patients who participated in the EF-14 trial. Methods: Biopsy patients of the EF-14 trial who exhibited radiological progression were included in this study (treatment: N=37/60, control: N=12/29). Volumes of enhancing tumor were segmented on T1-contrast MRIs at baseline and at progression. The tumor Specific Growth Rate (SGR) was calculated as: Specific_Growth_Rate=(ln(v0)-ln(v1))/dt. Here, v0 represents tumor volume at baseline, v1 represents tumor volume at progression, and dt represents the time to progression. This equation models tumor volume as increasing exponentially over time [3]. The distribution of growth rates in the treatment and control arms were compared. The analysis was restricted to biopsy-only patients since the definition of tumor volume is ambiguous in patients that underwent resection, as a large portion of the tumor has been removed. Results: The median growth rate was lower in the treatment arm than in the control. (control: 0.14±0.12 mL/month, TTFields -0.011±0.11 mL/month, p&amp;lt;0.008 Wilcoxon rank-sum). Discussion and conclusions: This study suggests that TTFields does indeed enhance local control of the tumor, significantly inhibiting the growth rate of the primary lesion. In this context, is worth noting that standard practice is to plan placement of the transducer arrays used to deliver TTFields in order to maximize dose delivered to the tumor. Thus, the results of this study support the hypothesis that adaptive treatment planning, in which the transducer array layout is periodically changed in order to dynamically target regions in which progression is observed, may help to improve patient outcomes.

Evaluation of ABO blood groups and blood-based biomarkers as a predictor of growth kinetics of renal angiomyolipoma.

The aim of our study was to investigate the impact of the ABO blood groups and blood-based biomarkers on the growth kinetics of renal angiomyolipoma (AML). A total of 124 patients with AML who were followed-up between 2010 and 2018 were retrospectively reviewed. The patients' characteristics were recorded, including age, body mass index (BMI), blood pressure, smoking history, and ABO blood group. Baseline laboratory test results, including serum creatinine, AST, ALT, platelet, neutrophil and lymphocyte count, were used to calculate the estimated glomerular filtration rate (eGFR), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and De Ritis ratio. The Cox regression analysis was used to evaluate the relationship between variables and tumor growth. The study population comprised 71 women and 44 men with a median age of 47.3 (28-65)years. Among patients classified according to the blood groups, no significant differences were observed regarding age, BMI, smoking history, co-morbidities, NLR, PLR, De Ritis ratio, eGFR, or tumor size and localisation. The mean growth rate from baseline to the last scan was 0.36 ± 0.27cm, 0.21 ± 0.21cm, 0.14 ± 0.11cm, and 0.19 ± 0.17cm for blood type O, A, B, and AB, respectively. In multivariate analysis, eGFR < 60 (p = 0.044), central tumor localisation (p = 0.030), presence of blood group-0 (p = 0.038), and De Ritis ratio ≥ 1.24 (p = 0.047) were statistically associated with tumor growth. Our study demonstrates that both the ABO blood groups and the De Ritis ratio might represent independent predictors of tumor growth rate in patients with renal AML.

Effect of nivolumab on tumor growth rate (TGR) in metastatic renal cell carcinoma (mRCC).

481 Background: Response assessment under immune checkpoint inhibitors is a challenge that RECIST criteria may not adequately reflect. TGR takes into account the pretreatment kinetics and allows dynamic assessments. How TGR varies under nivolumab remains unknown. We aim at describing the pattern of TGR changes during nivolumab treatment. Methods: We performed a central radiological review of all consecutive patients treated with nivolumab at Gustave Roussy within the GETUG-AFU 26 NIVOREN (EudraCT 2015-004117). Tumor response was assessed at week 8 and every 8-12 weeks subsequently using RECIST 1.1. TGR was computed for the pre nivolumab treatment (TGR pre) and at first (TGR N1) and second assessment (TGR N2) under nivolumab. Results: A total of 45 patients treated with nivolumab between Feb and Jul 2016 were reviewed. Median age at nivolumab start was 60 years-old, 74 % were male. Median number of prior lines of systemic therapies was 2. Median follow-up from nivolumab start was 6 months. TGR pre and TGR N1 were available in 39 patients. Overall, mean decrease in TGR N1 compared to TGR pre was 26%. Among 39 evaluable patients, 23 (59%) patients had a decrease in TGR N1 compared with TGR pre; while an increase was described in 16 (41%) patients. Only one patient out of 39 (2.5%) had a major increase of more than 50% in TGR N1 compared with TGR pre, and could be defined as a hyper-progressor. Consecutive TGR N1 and TGR N2 were available in 24 patients. There was a high correlation between TGR N1 and TGR N2 (r=0.7), suggesting that first evaluation of tumor kinetics adequately reflects subsequent response to nivolumab. However, 4/24 patients (17%) had an initial increase in TGR N1 with subsequent decrease in TGR N2, defining potentially the pseudo-progressors. Conversely, 6/24 patients (25%) had an initial decrease in TGR N1 before a rebound in TGR N2 suggesting a prompt acquired resistance to nivolumab. Conclusions: We report the first TGR assessment of mRCC patients under nivolumab. Overall, 59 % of patients had a decrease in TGR under nivolumab compared to pre nivolumab. TGR in patients with mRCC might provide early information about tumor response to nivolumab. Analysis extended to the entire study population and correlation with PFS and OS will be reported.

TARP vaccination is associated with slowing in PSA velocity and decreasing tumor growth rates in patients with Stage D0 prostate cancer

ABSTRACTT-cell receptor alternate reading frame protein (TARP) is a 58-residue protein over-expressed in prostate and breast cancer. We investigated TARP peptide vaccination's impact on the rise in PSA (expressed as Slope Log(PSA) or PSA Doubling Time (PSADT)), validated tumor growth measures, and tumor growth rate in men with Stage D0 prostate cancer. HLA-A*0201 positive men were randomized to receive epitope-enhanced (29-37-9V) and wild-type (27-35) TARP peptides administered as a Montanide/GM-CSF peptide emulsion or as an autologous peptide-pulsed dendritic cell vaccine every 3 weeks for a total of five vaccinations with an optional 6th dose of vaccine at 36 weeks based on immune response or PSADT criteria with a booster dose of vaccine for all patients at 48 and 96 weeks. 41 patients enrolled with median on-study duration of 75 weeks at the time of this analysis. Seventy-two percent of patients reaching 24 weeks and 74% reaching 48 weeks had a decreased Slope Log(PSA) compared to their pre-vaccination baseline (p = 0.0012 and p = 0.0004 for comparison of overall changes in Slope Log(PSA), respectively). TARP vaccination also resulted in a 50% decrease in median tumor growth rate (g): pre-vaccine g = 0.0042/day, post-vaccine g = 0.0021/day (p = 0.003). 80% of subjects exhibited new vaccine-induced TARP-specific IFNγ ELISPOT responses but they did not correlate with decreases in Slope Log(PSA). Thus, vaccination with TARP peptides resulted in significant slowing in PSA velocity and reduction in tumor growth rate in a majority of patients with PSA biochemical recurrence.

O-016 Exploratory analysis of tumor growth rate in patients with advanced gastrointestinal stromal tumors (GIST) treated with regorafenib in the GRID phase 3 trial

O-016 Exploratory analysis of tumor growth rate in patients with advanced gastrointestinal stromal tumors (GIST) treated with regorafenib in the GRID phase 3 trial

Small Renal Masses Managed With Active Surveillance: Predictors of Tumor Growth Rate After Long-Term Follow-Up

BackgroundThe purpose of the study was to evaluate the relationships between the patients' clinical characteristics and the growth pattern of SRMs, and to investigate the predictive factors of tumor growth rates in patients initially managed with AS. Materials and MethodsWe retrospectively reviewed data from our prospectively collected database of 70 patients diagnosed with 72 SRMs between 1996 and 2013. Clinical and demographic data, and linear and volumetric growth rates were recorded for each patient. A Pearson correlation test was used to evaluate initial tumor size and linear or volumetric growth rate. Logistic regression models were used to evaluate the predictive factors affecting tumor growth kinetics. ResultsThe mean age was 76 ± 6.8 years, and 47 (67.1%) of patients were male. The mean (± SD) and the median (interquartile range [IQR]) tumor size at presentation were 2.1 ± 1.3 and 2.7 (1.8-3.7) cm, respectively. The mean (± SD) and the median (IQR) linear growth rate were 0.5 ± 0.3 and 0.6 (0.4-1.5) cm per year, respectively. Patients treated with delayed surgery experienced a significantly greater mean linear growth rate (1.4 vs. 0.3 cm per year) than those observed in the AS group (P < .001). Male sex (HR, 1.70; P = .04) and symptomatic presentation (HR, 1.85; P = .02) were found to be significant predictors of tumor growth rates during AS. Conversely, age, Charlson Comorbidity Index, and initial tumor size failed to predict growth kinetics. ConclusionMale sex and symptomatic presentation are associated with faster growth rates in patients managed with AS after long-term follow-up.

A hypothesis about the potential role of statin administration as adjuvant treatment in the management of Merlin-deficient tumors

Merlin, a tumor suppressor protein, controls essential steps of cell cycle, and its deficiency results in cellular overgrowth, proliferation, angiogenesis, invasion and metastasis. Lack of Merlin is responsible for neurofibromatosis-2, most schwannomas, and many meningiomas and ependymomas. We hypothesize that there is a role for statins to ameliorate Merlin's deficiency in this set of tumors by inhibiting a number of Merlin's downstream effectors, the small Rho-GTP-ases, and we present the relevant data. The ultimate goal is to offer a medical therapy promising to halt or reduce the tumor growth-rate in patients harboring Merlin-deficient neoplasms and to provide an adjuvant systemic therapy for patients undergoing stereotactic radio-surgery and partial tumor resection.

Volumetric tumor growth in advanced non‐small cell lung cancer patients with EGFR mutations during EGFR‐tyrosine kinase inhibitor therapy

BACKGROUNDThe objective of this study was to define the volumetric tumor growth rate in patients who had advanced nonsmall cell lung cancer (NSCLC) with sensitizing epidermal growth factor receptor (EGFR) mutations and had initially received treatment with EGFR‐tyrosine kinase inhibitor (TKI) therapy beyond progression.METHODSThe study included 58 patients with advanced NSCLC who had sensitizing EGFR mutations treated with first‐line gefitinib or erlotinib, had baseline computed tomography (CT) scans available that revealed a measurable lung lesion, had at least 2 follow‐up CT scans during TKI therapy, and had experienced volumetric tumor growth. The tumor volume (in mm3) of the dominant lung lesion was measured on baseline and follow‐up CT scans during therapy. In total, 405 volume measurements were analyzed in a linear mixed‐effects model, fitting time as a random effect, to define the growth rate of the logarithm of tumor volume (logeV).RESULTSA linear mixed‐effects model was fitted to predict the growth of logeV, adjusting for time in months from baseline. LogeV was estimated as a function of time in months among patients whose tumors started growing after the nadir: logeV = 0.12*time + 7.68. In this formula, the regression coefficient for time, 0.12/month, represents the growth rate of logeV (standard error, 0.015/month; P &lt; .001). When adjusted for baseline volume, logeV0, the growth rate was also 0.12/month (standard error, 0.015/month; P &lt; .001; logeV = 0.12*months + 0.72 logeV0 + 0.61).CONCLUSIONSTumor volume models defined volumetric tumor growth after the nadir in patients with EGFR‐mutant, advanced NSCLC who were receiving TKI, providing a reference value for the tumor growth rate in patients who progress after the nadir on TKI therapy. The results can be studied further in additional cohorts to develop practical criteria to help identify patients who are slowly progressing and can safely remain on EGFR‐TKIs. Cancer 2013;119:3761–3768. © 2013 American Cancer Society.

Abstract 4571: Autologous TARP peptide vaccination is associated with slowing in PSA velocity and a decrease in tumor growth rate in patients with Stage D0 prostate cancer.

Abstract Background: T-cell receptor alternate reading frame protein (TARP) is a novel, immunogenic 58 amino acid protein that is over-expressed in ∼95% of prostate cancer and ∼50% of breast cancer specimens and hence is a good candidate for therapeutic vaccination. In mice the immunogenicity of HLA-A*0201 binding TARP peptides can be improved through epitope-enhancement achieved by amino acid substitutions that result in increased HLA binding affinity. We conducted a first-in-human study to determine the safety and immunogenicity of TARP peptide vaccination and its impact on the velocity of PSA rise (expressed as slope log (PSA) or PSA doubling time (PSADT)) and tumor growth rate in men with Stage D0 prostate cancer. Methods: HLA-A*0201 positive men were randomized to receive epitope-enhanced (29-37-9V) or wild type (27-35) TARP peptides administered as a peptide emulsion with Montanide ISA 51VG plus GM-CSF (Arm A) or as an autologous peptide-pulsed dendritic cell vaccine (Arm B). Vaccines were administered q 3 weeks for a total of 5 vaccines with an optional 6th dose of vaccine at 36 weeks based on immune response or PSADT criteria and a booster dose of vaccine for all patients at 48 and 96 weeks. Results: A total of 41 patients (n = 21 Arm A, n = 20 Arm B) enrolled, with a median on study duration of 75 weeks as of 07/31/12. Baseline cohort characteristics (median): age 62 yrs, PSA 3.44, Gleason Score 7, ALC 1270, CD4%/absolute 42.5%/547 cells/mm3, 25-OH vitamin D level 28, with 30 of 41 (73%) s/p radical prostatectomy and 26 of 41 (63%) s/p EBRT for PSA biochemical recurrence. TARP vaccination was safe and well tolerated with adverse events limited to local injection site reactions &amp;lt; Grade 2. Twenty-eight of 39 patients (72%) reaching 24 weeks and 23 of 31 (74%) reaching 48 weeks were documented to have a decreased slope log PSA compared to their pre-vaccination baseline (p=0.0012 and p=0.0004 for overall changes in slope log PSA, respectively); there was no statistically significant difference between the two arms, although only the DC arm was significant at 48 wks on its own. TARP vaccination also resulted in a 50% decrease in calculated tumor growth rate constant: pre-vaccine g = 0.0042/day, post-vaccine g = 0.0021/day (p=0.003). TARP-specific IFN-γ ELISPOT responses were detected in the majority of subjects but did not correlate with observed decreases in slope log (PSA). Citation Format: Lauren V. Wood, William L. Dahut, Antonio Fojo, James L. Gulley, Ravi Madan, Philip Arlen, Howard L. Parnes, Brenda D. Roberson, Seth M. Steinberg, Masaki Terabe, Julia Wilkerson, Ira Pastan, Jay A. Berzofsky. Autologous TARP peptide vaccination is associated with slowing in PSA velocity and a decrease in tumor growth rate in patients with Stage D0 prostate cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4571. doi:10.1158/1538-7445.AM2013-4571

Mapping tumor growth rates in patients with malignant gliomas: A test of two algorithms

Mapping tumor growth rates in patients with malignant gliomas: A test of two algorithms

Conservative management of acoustic neuroma: an outcome study.

This study analyzed selection criteria, clinical outcome, and tumor growth rates in patients with acoustic neuromas in whom the initial management strategy was observation. A retrospective review of patients with conservatively managed unilateral acoustic neuromas was conducted. Minimum follow-up was 6 months. Patients with neurofibromatosis Type II were excluded. Differences in tumor growth rates were analyzed by use of the Wilcoxon rank sum test. Sixty-eight patients (31 men and 37 women) with a mean age of 67.1 years were followed for an average of 3.4 years after diagnosis. The reasons for a trial of observation included advanced age (55%), patient preference (21%), minimal symptoms (9%), poor general medical condition (7%), asymptomatic tumor (4%), and tumor in the only hearing ear (4%). Fifty-eight patients (85%) were successfully managed with observation alone. Ten patients (15%) ultimately required treatment (nine received microsurgical treatment and one patient underwent radiosurgical intervention) at a mean time interval of 4.0 years after diagnosis. Forty-eight tumors (71%) showed no growth and 20 (29%) enlarged during the study period. The mean tumor growth rate at the 1-year follow-up was significantly higher in the group requiring treatment (3.0 mm) than in the group not requiring treatment (0.36 mm) (P < 0.0001). Thus, the tumor growth rate at the 1-year follow-up was a strong predictor of the eventual need for treatment. Observation is a reasonable management strategy in carefully selected patients with acoustic neuromas. Diligent follow-up with serial magnetic resonance imaging is recommended, because some tumors will enlarge to the point at which active treatment is required.

Evaluation of tumor growth rate in patients with early gastric carcinoma of the elevated type

The growth rates of elevated-type early gastric carcinoma in 12 patients were determined chronologically using serial radiographs. Eight progressed from an early to an advanced stage during periods of observation ranging from 4-82 months (mean 31.7 months), while four patients were still in an early stage at final examination, despite an increase in tumor size. The tumor volume doubling months) but varied considerably among patients. Aggressive endoscopy should be performed for all elevated lesions of the stomach because they can harbor malignancy; some can grow rapidly as reported here.